Spinal Cord Injury: Where Level Matters - A Study of Cardiac Output Kinetics During Exercise

To investigate the cardiac output responses (Qt) relative to oxygen consumption (VO2) in individuals with incomplete SCI (iSCI) during walking.

This cross-sectional pilot study included 11 participants: 4 with tetraplegia (TG, age 41 ± 21 years), 4 with paraplegia (PG, age 47 ± 19 years), and 3 able-bodied controls (HC, age 27 ± 8 years). Participants performed a constant-workload treadmill test at a self-selected speed. Qt was measured using impedance cardiography, and VO2 was assessed via pulmonary gas exchange analysis. Data were reported as means ± SD. One-way analyses of covariance (ANCOVA) with age speed as covariates was used to investigate differences across the 3 groups. 

The treadmill self-selected walking speed was significantly different across the group. It was significantly lower in tetraplegic subjects compared to PG and HG (TG at 0.6 mph and PG at 0.9 mph vs.1.5 mph, p=0.03). Despite HC walking at a greater speed (1.5 mph vs. TG at 0.6 mph and PG at 0.9 mph), Qt and VO2 amplitudes did not differ among groups. Qt kinetics, represented by the time constant (τ), were significantly prolonged in TG (50 ± 13s) compared to PG and HC (17 ± 4s and 6 ± 4s, respectively). VO2 kinetics during phase II were similar among groups, but effect sizes indicated potentially meaningful slowing in TG and PG compared to HC.

These findings suggest that sympathetic innervation influences Qt kinetics in a lesion-dependent manner. The observed differences in Qt kinetics among groups may be attributed to the varying degrees of sympathetic disruption. Tetraplegics, with greater disruption of sympathetic outflow, demonstrated slower Qt adaptation to increased metabolic demand.. However, the trend towards slower VO2 kinetics in the tetraplegic and paraplegic groups warrants further investigation, as it may indicate subtle impairments in muscle oxidative metabolism. The findings suggest a lesion-dependent impairment in Qt adaptation, with individuals possessing higher-level injuries demonstrating slower Qt responses. This mismatch between Qt and VO2 may contribute to the exercise intolerance commonly observed in this population. Further research is needed to  develop targeted interventions aimed at improving exercise tolerance in individuals with iSCI.

The present study underscores the importance of considering the level of lesion when examining cardiovascular responses to exercise in individuals with iSCI. Elucidating the specific impairments in cardiovascular control following SCI could inform the development of targeted therapeutic interventions. Thus, the present findings suggest that cardiac output kinetics during exercise may serve as a valuable prognostic indicator that may signal a higher risk for future cardiovascular complications, warranting closer monitoring and more preventive strategies.